Nutritional selenium deficiency is found in certain parts of the world and in patients on specialized diets or receiving total parenteral nutrition. Selenium deficiency results in a deficiency of glutathione peroxidase. The overall objective of this investigation is to relate the development of selenium deficiency and its repletion to changes in red blood cell, granulocyte, platelet and plasma glutathione peroxidase and how this effects cell function and the metabolism of and sensitivity to H2O2. Patients receiving total parenteral nutrition will be examined as will rats fed a selenium deficient diet. Repletion with intravenous selenous acid will be given those patients found to be significantly selenium deficient. Variable repletion will be given animals. The effect of glutathione peroxidase deficiency on red cell redox state, granulocyte phagocytosis and platelet aggregation will be assessed. The ability of these cells to function after being stimulated with an H202 generating system will also be assessed as will the ability to metabolize exogenous H202. The effect of glutathione peroxidase deficiency on glutathione metabolism will also be determined. The nature of the protein of glutathione peroxidase will be studied. By utilizing BCNU to inhibit glutathione reductase, the combined deficiency state will be studied. The results of these studies will hopefully be applicable to all instances of selenium deficiency.